Spasticity
Spasticity is a classical neurological symptom after brain injury. Simply, spasticity means that the resistance to passive movement in a body part increases, as muscles get stiffer and the normally inhibited stretch reflexes become hyperactive. Spasticity is also velocity dependent, so that a faster passive movement results in greater resistance to movement (Lance, 1980). It is occurs in about one fourth of all stroke patients (Sommerfeld et al, 2004; Watkins et al, 2002). Depending on the severity level it leads to functional impairments, pain, disability and reduced autonomy. Despite our lack of knowledge of the exact mechanisms, spasticity is treated with a variety of physical interventions (e.g. stretching, splinting, orthoses) and medication (e.g., botulinum toxin injections in the muscle, known as “Botox”) in the clinical setting. In severe cases surgery may be indicated to help gain the joint range of motion (e.g., in spastic cerebral palsy).
There are (1) non-neural and (ii) neural components which contribute to the increased resistance to passive movement. The non-neural components include: spastic muscle cell atrophy and fibre type transformation (Dietz et at, 1986); reduced sarcomere length and changed muscle and extra cellular viscoelastic properties (O'Dwyer et al, 1996; Singer et al, 2003; Friden and Lieber, 2003; Olsson et al, 2006). Neural components include: reduced stretch reflex thresholds and increased gain of the stretch reflex (Thilmann et al, 1991; Ibrahim et al, 1993; Pierrot-Desseilligny and Burke, 2005; Nielsen et al, 2007).
Clinical Methods
Clinical practice of today lacks effective methods to reduce spasticity. Instruments which can be used for quantification of muscle tone are therefore needed. Clinical measurement of spasticity, by doctors and physical therapists, is today performed in a subjective way using a 5-point rating scale. The limb is manually moved passively, one feels the resistance and thereafter one rates it according to the Modified Ashworth rating scale (Bohannon and Smith, 1987).
The reliability of a diagnosis would increase if the clinical measurement was objective. Treatment and rehabilitation could be better targeted if the diagnosis could separate and estimate the influence of the mechanical muscle components and the neural stretch reflex components.
Experimental Studies
Early experimental studies of both the non-neural and neural components did not examine how these components related to other functional measures (Thilmann et al, 1991; Ibrahim et al, 1993). These studies used electromyography (EMG) to quantify neural activity in spasticity. However, EMG measurements are cumbersome and inter-subject comparisons remain problematic (Katz and Rymer, 1989). More recently some studies have examined the relationship between both non-neural and neural components and clinically assessed function at the ankle (Huang et al, 2006) and in the hand (Kamper et al, 2000+2003). However, these studies used specific in-house equipment (EMG and torque measures) that would be difficult to use routinely in the clinic. In addition, Kamper et al (2003) used local anaesthesia in finger muscles in order to isolate neural contribution to passive movement resistance. This method is therefore not suited as an easy-to-use clinical tool to quantify non-neural and neural contributions to increased passive movement resistance after stroke.
Experimental Studies Using Models
As there are multiple mechanical and neural factors which contribute to the passive movement resistance modelling can aid understanding of how these factors interact (Koo and Mak, 2006; He, 1998). Models have used joint position (He, 1998; Feng and Mak, 1998), EMG (Feng et al, 1999) or torque (Schmit et al, 1999; Koo and Mak, 2006) as input. Studies using joint position during passive movement indicate that posture and muscle length may effect measurements of spasticity (He, 1998) and that decreased stretch reflex thresholds and increased reflex gain may explain reduced movement during the pendulum test in the elbow in spastic patients (Feng and Mak, 1998). The importance of reflex activity was shown by Feng et al (1999) who were able to predict the passive movement trajectory by using EMG as model input. Koo and Mak (2006) performed detailed modelling of mechanical and neural factors effecting passive movement torque. A sensitivity analysis indicated that muscle spindle static gain and motoneuron pool threshold were the most sensitive parameters that could affect the stretch reflex responses of the elbow flexors. This was followed by motoneuron pool gain and spindle dynamic gain. The above results illustrate how mathematical modelling of the neuro-biomechanics at a joint is useful for understanding how mechanical and neural factors change with spasticity. However, none of the above studies investigated how the modelled factors related to function. In general, the modelling was detailed and time consuming making use of such modelling difficult in the clinical setting.
In order to develop an easy-to-use clinical spasticity measurement tool we have therefore developed a new method for separate quantification of non-neural and neural contributions to passive movement resistance. Different resistance characteristics during passive hand movements at different velocities are used to obtain values of non-neural and neural contributions via a mathematical model of the neuro-biomechanics of the human wrist (see Method for details).
The patent document US-A1-2007/0027631 describes an apparatus and method for evaluating a hypertonic condition such as spasticity in a movable extremity. The apparatus includes an accelerometer, a gyroscope, and a sensor adapted for quantifying force or pressure. The apparatus and method make use of a remote device 12 (e.g. see FIG. 5) which has a case 52, a strap 54 coupled to the case 52 so that the remote device 12 can be attached to the limb of a patient (see FIG. 6). An accelerometer 56, a gyroscope 58, and a pressure transducer 60 are mounted and connected on a circuit board 66. Also mounted and connected on the circuit board 66 are the power supply 34 and the electronic circuit devices 64 for processing and transmitting the data signals to the host processor 14.
The patent document WO-A1-2006/102764 describes a method and apparatus that advantageously measures spasticity in a reproducible way. In FIG. 1 an arm 10 is shown in which the elbow (the joint) is bent at an angle A. A joint angle sensing device such as a goniometer 12 is attached to the arm to provide angle measurements and muscle activity is monitored by an EMG 14 comprising electrodes 15. The data is processed by data processor 16 to assess spasticity by computing the angle A at which the onset of the stretch reflex (SR) is triggered. The results may be compared to results obtained for normal individuals or individuals with similar or different diseases.
Other Patents Related to Spasticity
                1. Apparatus and method for evaluating a hypertonic condition, Inventor: CABRERA MICHAEL NORMANN B (US); NORRIS JAMES A (US) Applicant: EC: IPC: G01 N33148; G01 N33/50; G01 N33148 (+1), Publication info: US2007027631-2007-02-01. [Differs from Spastiflex in the following: uses position, velocity, gyro, acceleration does not differentiate mechanical and neural contributions to muscle tone. Similarities: measures force, uses model        2. Method and apparatus for resistive characteristic assessment, Inventor: ENGSBERG JACK R (US); ENGSBERG DAVID P (US); (+1), Applicant: BARNES JEWISH HOSPITAL, EC: IPC:A61B5/22; A61B5/22, Publication info: US2007012105-200701        3. METHOD AND APPARATUS FOR DETERMINING SPASTICITY, Inventor: LEVIN MINDY (CA); FELDMAN ANATOL (CA); (+1), Applicant: VALORISATION RECH SOC EN COMMA (CA); UNIV MCGILL (CA); (+3), EC: A61B5/0488; A61B5/11, IPC: A61B5/11; A61B5/0488; A61B5/11 (+1), Publication info: W02006102764-2006-10-05.        4. Botulinum toxins for treating muscle spasm Inventor: AOKI ROGER K (US); GRAYSTON MICHAEL W (US); (+2), Applicant: ALLERGAN INC (US), EC: IPC: A61 K38148; A61 P21102; A61K38/43 (+3), Publication info: EP1486214-2004-12-15. [Common treatment of spastic muscles]        5. METHOD FOR SIMULATION OF SPASTICITY, Inventor: KARAMYSHEV VASILIJ D (SU), Applicant: KH MED INST (SU), EC: IPC: G09B23/28; G09B23/00; (IPC1-7): G09B23/28, Publication info: SU1649599-1991-05-15 [Document available In Russian language only]        6. METHOD OF MEASURING AND RECORDING DEGREE OF LIMBS SPASTICITY, Inventor: FRANEK ANDRZEJ; GORECKI IGNACY; (+1) Applicant: GORNICZE CT REHABILITACJI LECZ (PL), EC: IPC: A61B; (IPC1-7): A61B, Publication info: PL270374-1989-01-05 15 [Descriptive documents not available]        7. Quantification of muscle tone, Uppfinnare: KANDERIAN SAMI S (US); GOLDBERG RANDAL P (US); (+4) Sökande: EC: A61B5/0488; A61B5/22D IPC: A61 B5/0488; A61B5/22; A61B5/0488 (+3), Publication information: US2002156399-2002-10-24 [Differs from Spastiflex in the following: no estimation of reflex: “moving the patient's wrist in a non-sinusoidal and non ramp trajectory and determining the stiffness, viscosity and inertial parameters using the following relationship’]        